CHRONIC INFECTIONS OF JAWS

Presented by Dr. Mohammed haneef

INTRODUCTION ANATOMY OF BONE

TYPES OF INFECTIONS AFFECTING BONE PERIOSTITIS OSTEITIS OSTEOMYLTIS

HISTORY CLASSIFICATION ETIOPATHOGENESIS PREDISPOSING FACTORS MICROBIOLOGY TYPES AND CLINICAL FEATURES INVESTIGATIONS MANAGEMENT

Bone is a connective tissue in which cells are arranged at regular interval in a matrix.

The matrix is impregnated with calcium phosphates & Calcium hydroxide salts.

Adult bone consists of • 30-40 % Collagen.

• 60-70% minerals.(Excluding 25-30% of water).

• In Maxilla-

• Cortex is thin, In anterior region Spongy part is well Developed.

• Highly vascularised

• In Mandible-

• Well developed

• Periosteum and Cancellous

• A solid cortex.

• Two sources of blood supply

Bacterial, Trauma, Dental infection(A)Acute Periostitis- Fulminating infection

Exudates separates the periosteum From bone

OMLC/F- Localized-Periosteum over infected tooth involved. Suppurative- Swelling of the face, Pain, Tenderness. Sever stage- Trismus, loosening of teeth, Sinus tract &

Pus discharge, Chills, Fever.Treatment:Early Stage- Antibiotics, Extraction of offending teeth, -Hot moist packs. Late Stage- I & D.

(B) Chronic Periostitis / Garre’s Osteomyelitis:Follows the Acute phase

Osteogenic activity may be stimulated

New bone formation, also called Periostitis Ossificans.

R/F: Increased radio-opacity, & thickening of periosteum, Bone deposition at periphery.

Treatment:-Antibiotics & Hot moist Packs.

If adjacent bone is involved then Seqeustrum is removed.

• Debridement

• Drainage.

(A) Suppurative Osteitis:

Can arise from

• Odontogenic infection of carious tooth.

• Pericoronal Infection From Erupting 3rd molar.

That's why classified as Dentoalveolar Abscess.

It may destroy the bone extensively but remains walled off & doesn’t Spread.

R/F: • Circumscribed osteolytic area, • without definite cortical border.• Sometimes irregular area of

Osteolysis.

• Bone formation as a result of inflammation.

• Infections & Circulatory Conditions are responsible (Heiss 1954)• In some cases- process represents repair following the destruction of the

bone.

• In other cases- an initial bone production after osteoblast activation by mild & chronic infection.

Cortical type of bone is produced.

in marrow space.

Elimination of spongiosa.

cellular infiltration in remaining marrow space.

(process is inflammatory)

(B) Sclerosing (Condensing) Osteitis:

R/f: Radiopaque irregular outline

with peripheral extensions.

C/f: Neurologic pain.

Boring character.

T/t: -Antibiotics

-Extraction of associated

tooth.

Sever pain –

• Decompression of the Inferior alveolar

• nerve.

• Excision of the sclerosed area.

In Greek osteon means bone myelos means marrow itis means inflammation

• OML is defined as an inflammatory condition of bone primarily involving soft tissues{ARCHER 1975}

• Extensive inflammation of bone involving cancellous portion{LASKIN}• Inflammation of bone marrow with a tendency to progression, involving

adjacent cortical plates & periosteum tissues.{Michael miloro}

• An inflammatory disease of bone that begins as a bacterial infection of cancellous vascular spaces, comprising the haversian circulatory systems & eventually extending to involve cortex & periosteum.{OMSCNA 1991}

“ Osteomyelitis may be defined as an inflammatory condition of bone, that begins as an infection of medullary cavity and haversian systems and extends to involve the periosteum of the affected area ”

Reference Classification Classification Criteria

Topazian RGOsteomyelitis of the Jaws. In Topizan RG,Goldberg MH (eds): Oral and MaxillofacialInfections.Philadelphia, WB Saunders 1994,Chapter 7, pp 251-88

I. Suppurative osteomyelitis1. Acute Suppurative osteomyelitis2.Chronic Suppurative osteomyelitis.-Primary chronic Suppurative OML-Sec. chronic Suppurative OML3. Infantile osteomyelitis.

II. Nonsuppurative osteomyelitis1. Chronic sclerosing osteomyelitis– Focal sclerosing osteomyelitis– Diffuse sclerosing osteomyelitis2. Garrè's sclerosing osteomyelitis3. Actinomycotic osteomyelitis4. Radiation osteomyelitis and necrosis.

Classification based on clinical picture,radiology, and etiology(specific forms such as syphilitic,tuberculous, brucellar, viral, chemical,Escherichia coli and Salmonellaosteomyelitis not integrated in classification)

Reference Classification Classification criteria

Hudson JWOsteomyelitis of the jaws: a 50-yearperspective.J Oral Maxillofac Surg 1993Dec;51(12):1294-301

I. Hematogenous osteomyelitis

II. Osteomyelitis secondary to a contiguous focus of infection.

III. Osteomyelitis associated with or without peripheral vascular disease.

Classification based on pathogenesis.From Vibhagool 1993

Reference Classification Classification criteria

Hudson JWOsteomyelitis of the jaws: a 50-yearperspective.J Oral Maxillofac Surg 1993Dec;51(12):1294-301

I. Anatomic TypesStage I: medullar osteomyelitis –involves medullar bone withoutcortical involvement; usually Hematogenous.Stage II: superficial osteomyelitis –less than 2 cm bony defect withoutcancellous boneStage III: localized osteomyelitis– less than 2 cm bony defect onradiograph, defect does not appearto involve both cortices.Stage IV: diffuse osteomyelitis defect greater than 2 cm. Pathologicfracture, infection, nonunion.II. Physiological classA host: normal hostB host: systemic compromised host,local compromised hostC host: treatment worse than disease.

Dual classification based on pathologicalanatomy and pathophysiologyFrom Vibhagool 1993 and Cierny 1985

• Lytic

• Sclerotic

• Mixed &

• Sequestrum pattern .

(Indian Journal Of Radiology & Imaging1993)

The patients were classified based on 5 disease stages: • stage 0, potential osteomyelitis with bone contamination; • stage I, early or acute osteomyelitis;

• stage II, intermediate osteomyelitis with subperiosteal abscess;

• stage III, late or chronic osteomyelitis with sequestrum and subdivided into curable (IIIa), controllable (IIIb) and complicated (IIIc); and

• stage IV, compound osteomyelitis either anatomical (IVa) or physiological (IVb).

(East African Medical Journal, 2003 (Vol. 80) (No. 7) 373-378

IMMUNOCOMPROMISED PATIENTS

• Diabetes • Leukemia• Severe anemia, • Malnutrition, • Chronic alcoholism, • Sickle cell anemia and • Febrile illness such as

Typhoid.)• Agranulocytosis

ALTERATION IN JAW VASCULARITY

• Radiation, • Osteoporosis, • Paget`s disease, • Fibrous dysplasia, • Bone Malignancy

and Bone Necrosis caused by Mercury, Bismuth and Arsenic

Acute inflammation ( edema, pus)

Increased intermedullary pressure

Vascular collapse (stasis, ischemia of bone)

Avascular bone

Pus organism extention

Haversian system/ nutrient canal involvement

Elevation of periosteum

Disruption of periosteal blood supply

Avascular infected bone

• Pathogenesis can be divided into 4 phases:• Microbial adherence and invasion:• Mechanisms of tissue destruction and bone death:• Mechanism of microbial persistence:• Responses to infection

• Osteomyelitis --- opportunistic disease as presented by the host to the pathogenic microbe.

• Odontogenic infections.• Trauma. • Infections of orofacial regions. • Hematogenous spread.

•Caused primarily by streptococci (alpha hemolytic)

•Oral anaerobes particularly Bacteriodes fragilis, Bacteriodes melanogenicus and Fusobacterium, peptostreptococcus.

•Staphylococcus aureus.

• Capable of adhering to bone, tend to develop resistance to antimicrobial therapy

• Capability to survive intracellularly

•In addition Mycobacterium tuberculosis, Treponema palladium and Actinomyces israelli produce certain specific forms of osteomyelitis.

• Findings suggestive of pure anaerobic or mixed aerobic/anaerobic infections

• Mandible is affected more because of the dense, poorly-vascularised cortical plates and the single blood supply from the inferior alveolar neurovascular bundle.

• The extensive blood supply of the maxilla makes it less prone to ostemyelitis when compared to the mandible.

• The thin cortical plates and the porosity of the medullary portion preclude infections from becoming contained in the bone and facilitate spread of edema and purulent discharge into adjacent tissues.

Dentomaxillofacial Radiology (2005) 34, 86-90

• May involve maxilla or mandible • Common in infants• In maxilla it is fairly well localized, where as in mandible it

tends to be more diffuse and wide spread.• Staph. Aureus or Pyogenes is most commonly found, but

spirochetes or gram –ve bacteria may also be present.Clinical Features:• Severe pain, malaise and fever.• Regional lymphadenopathy.• Elevated WBC count.• Teeth involved may become loose and sore.• Paresthesia or anesthesia of lip.• Trismus may be present.

1. Primary – resulting from relatively less virulent organisms.

2. Secondary – occurring after acute phase when treatment did not succeed in eliminating the infection.

Clinical Features:

• The arbitrary time limit to differentiate chronic from acute osteomyelitis is one month.

• Dull aching pain and minimal tenderness.

• Non healing bony and overlying soft tissue wounds with induration of soft tissues.

• Intra oral or extra oral draining fistulae.

• Thickened or wooden character of bone.

• pathological fractures.

• Sterile abscesses (Brodies abscess) common in long bone, rare in jaws.

• Loose and sensitive teeth.

• Paresthesia or anesthesia is common.

• Enlargement of bone due to subperiosteal new bone deposition.

• Radiopaque sequestra (arrow) surrounded by the radiolucent suppuration.

• Worm-eaten appearance of the body of the mandible. Radiopaque sequestra

surrounded by the radiolucent suppuration and a radiopaque involucrum.

Rare type seen in infants maxilla• May be caused due to

perinatal,trauma, or due to contaminated nipples or finger in mouth, it is also believed to occur by hematogenous route (streptococcus).

• May have sudden onset with high fever, rapid pulse, vomiting, delirium, and prostration.

i. Chronic Focal Sclerosing Osteomyelitis

ii. Chronic Diffuse Sclerosing Osteomyelitis

2 ) Chronic Focal Sclerosing Osteomyelitis

• Usually due to high tissue resistance or low grade infection.

• Mandibular 1st molar is most common.

• Radiograph shows well- circumscribed radio opaque mass of sclerotic bone surrounding and extending below one or both roots.

• Should differentiate from benign cementoblastoma.

• Proliferative reaction of bone to a low grade infection.

• Older age group, especially in the edentulous mandible.

• More in blacks, especially females.• On occasion there may be acute

exacerbation and mild suppuration.• Radiologically mimics pagets

disease ‘cotton wool’ appearance.• mosaic pattern’, indicating

repeated periods of resorption and repair.

• Trebaculae are bordered by active layer of osteoblasts and inflammatory infiltrate.

• Described by Carl Garre in 1893.• Focal gross thickening of

periosteum of bone, with peripheral reactive bone formation.

• Almost always in children or young adults.

• Mandible is commonly involved.• Radiograph-- duplication of

cortical layer. • ‘onion skin’ appearance.

• Term was common in pre antibiotic era.

• After many years of chronic phase the original cortex is lost, there is much subperiosteal new bone and even hypercementosis of involved teeth resembles pagets disease.

• There is recurrent flares of infection.

In radiograph • blurring of corticomedullary bone border,• obliteration of marrow spaces and • poor remodeling of the external contour of the bone.

Here one should wait until the infected bone has completely separated and ward off by granulation tissue and then remove, in order to avoid the risk of infecting adjacent sclerotic bone and starting a fresh cycle.

Syphilitic osteomyelitis of the palate. The gummatous destruction has produced a palatal perforation.

Radiograph :The perforation which is the site of gumma of the hard palate produces a radiolucency which may be mistaken for amedian palatine cyst.

•Usually hematogenous spread when blood borne bacilli lodge in cancellous bone.•May also spread to bone by direct inoculation of bacilli into oral mucosa due to an ulcer or via a tooth socket.•The typical reddened abscess with no raise in local temperature occur i.e. ‘cold abscess’.•The lesion is located centrally.•The patient present only with swelling and no draining sinus, mimics parotid swelling this is called ‘lumpy jaw’•"worm eaten“appearance•Spiral CT showing osteolytic lesions of the mandible with bony fragmentation and surrounding soft tissue abscess with right submandibular lymphadenopathy.

Drugs Regime

Intensive

Treatment

Isoniazid

Rifampicin

Ethambutol

Pyrizinamide

300mg/day-4 months

15mg/kg body wt-4 months

25mg/kg-2months later15mg/kg

5-15g/day-4 months

Continuati-on phase

Isoniazid

Rifampicin

Ciprofoxacin

300mg/day-4 months

15mg/kg body wt-4 months

Panoramic radiograph showing ill-defined lytic area extending posterioinferiorly from primary right first molar to permanent right first molar.

FNAC showing granulomatous areas with characteristic Langhans’ giant cells and epitheloid cells surrounded by lymphocytes and plasma cells.

• A. Israeli.• Jaws are involved in cervicofacial type, especially

mandible.• Clinically soft or firm tissue masses on the skin,

which are purplish, dark red, oily with small zones of fluctuations.

• Spontaneous drainage of serous fluid containing yellowish granular material called ‘sulphur granules’ which represent colonies of bacteria.

• Radiographicaly mandible is thickened and ‘honey combed’ by narrow tracts in granulation tissue.

• Penicillin is the drug of choice • Treatment: Penicillin G,10-20 million

units/day IV for 4-6 weeks, followed by Penicillin V, 1g 4 times/day for 6-12 months.

• OR

• Ampicillin 50mg/kg/day IV for 4-6 weeks, then Amoxicillin 500mg 3 times/day for 6-12 months.

• Allergic to penicillin----- Doxycycline 100mg BD/day for 6 months.

Differential diagnosisOsteogenic sarcoma

• Permeative lesion borders,

• stippled bone pattern,

• destruction of Cortical outlines,

• perpendicular spiculations of periosteal new bone,

• destruction of lamina dura,

• and widening of the entire periodontal ligament space

Fibrous dysplasia• Superior displacement of the

mandibular canal and• In the absence of these

findings, • displacement of the sinus

cortex,• alteration of the lamina dura to

the abnormal bone pattern, and • narrowing of the periodontal

ligament space

Histopathology : • Blood and aspirate culture.• FNAC (infants.)• Samples for culture should be taken from infected

cavity wall, sequestrum, granulation tissue, involucrum and sinus tract (misleading).

• Organism can be identified and tested for antibiotic sensitivity.

• In acute form there will be elevated PMN cells.• But in chronic form some times may be culture –ve

and show only plasma cells and lymphocytes.• Distinctive histology may be seen in M.Tuberculosis

infection, like caseation and granulomatous lesion.

Blood Tests:• In acute presentations there is raised white cell

count (PMNs), C- reactive protein and ESR.

The Erythrocyte Sedimentation Rate (ESR):   When inflammation is present in the body, proteins are produced by the liver and the immune system . increased presence of these proteins will cause red blood cells to stick together in solution ,sedimentation rate is increased. many possible causes of an elevated sedimentation rate, this blood test is done with other tests to confirm a diagnosis such as a chronic osteomyelitis.

C-reactive protein (CRP): “acute-phase protein” synthesized by the liver. as an early defense system against infection.  It is a protein found in the blood, the levels of which rise in response to inflammation due to trauma, infection or serious illnesses.

In chronic phase there will be modestly raise in CRP, but ESR is often very high. 

• Nearly 30-60 % of mineral loss is required for significant radiographic changes.

• The full extent of bone destruction cannot be determined radiographicaly until 3 weeks after initiation of osteomyelitic process.

• Radiographic process lag behind the actual clinical situation.

•Takes 3 weeks to develop.

•So in acute osteomyelitis there is no much changes seen in plain x-rays, except for some times the individual trabaculae become fuzzy and indistinct.

•Well established osteomyelitis can be identified in radiographs by criteria given by Worth in 1969:

• Scattered areas of bone destruction, separated by variable distances. The appearance is one of increased radiolucency, which may be uniform or patchy.

• “moth–eaten” appearance, because of enlargement of medullary spaces and widening of Volkmann's canals.

• Bone destruction of varied extent in which there are ‘sequestra’ with a trabecular pattern and marrow spaces.

• A sheath of new bone, ‘involucrum’, is often found separated from sequestra by a zone of radiolucency.

• Can identify collection of fluid (pus) in the soft tissues and adjacent to bones can also be used for ultrasound guided aspiration.

• Scintigraphy using 99m Tc methylene diphosphonate can be done.

• PET scan can be done using radioisotopes like gallium or indium- labeled white cells which is less sensitive but more specific.

• useful in determining the presence of reactive bone, thus it is helpful in the diagnosis of bone diseases.

• (Tc99m) labeled diphosphonates are given intravenously--- accumulates in areas of increased osteoblasts activity (reactive new bone formation and increased blood flow).

The images obtained are • immediate (flow), • 15 minute (blood pooling), and • 4 hour (bone imaging) • osteomyelitis results in intense uptake in all 3 phases.

for acute osteomyelitis --almost 95% and findings generally are positive in 2-3 days of infection

Three-phase bone scanThree-phase bone scan

In--uses white blood cells labeled with radioactive indium as the tracer.

• used for the diagnosis of osteomyelitis at sites of fracture nonunion.

• Scintigraphy cannot distinguish between reactive bone associated with osteomyelitis and that seen in conditions as fibrous dysplasia.

• Here the patient’s own W.B.C are labeled in vitro and reinjected. Imaging is performed 8 to 24hrs after the injection, during which time. It is the most sensitive test and specific test for infections.

• Gallium citrate scanning an analog of calcium and iron and attaches to transferrin to accumulate at sites of inflammation.

• Dual tracer scans --examinations combine an inflammation imaging tracer (indium or gallium) with an "anatomic" tracer (either technetium bone scan or technetium sulfur colloid marrow scan), with images being collected either sequentially or simultaneously.

• Magnetic resonance imaging (MRI) is able to depict the bone marrow inflammation itself. Therefore, it has been described to be of value in defining the extent of the inflammatory process and in distinguishing OM from cellulitis.

• CT scan: accurate for detecting cortical destruction, intraosseous gas, periosteal reaction, and soft tissue extension.

• (A) Defect in the trabecular bone (arrow).

• (B) Osteosclerosis (arrow) and thickening of cortical bone (arrowhead).

• (C) Defect in the cortical bone (white arrow), periosteal reaction (white arrowhead) and osteosclerosis (black arrow).

• (D) Sequestrum (arrow) and thickening of the cortical bone (arrowhead).

• (E) Periosteal reaction (arrowhead) and defects of the cortical bone (arrows).

• (F) Change in the bone width (between arrows) Dentomaxillofacial Radiology (2005)

34, 86-90

• Image hard tissues in the maxillofacial region.

• capable of providing images of <0.5mm resolution that are of high diagnostic quality, with shorter scanning times (10–70 s).

• and considerably lower doses of radiation than conventional CT.

• Three-dimensional volumetric surface reconstructions showing the topography of the osteomyelitic defect used to plan the resection.preoperatively planned resection borders (dotted lines) were calculated by reference to the extent of the lesion measured from axial and cross-sectional images.

A. Conservative

B. Surgical

• Supportive therapy- e.g. nutrition.

• Blood transfusion- if anemic.

• Control of pain- using analgesics and sedatives.

• Antimicrobial agents.

CONSERVATIVE MANAGEMENTCONSERVATIVE MANAGEMENT::

• Penicillin remains the time- honoured antibiotic of choice for osteomyelitis.

• Initially gram stain guided empirical therapy is started usually with penicillin.

• Then after obtaining culture and sensitivity report specific therapy is started.

Regime 1: for hospitalized/medically compromised patient IV is given:

when improved for 48-72 hrs switch to

OR

when improved for 48-72 hrs switch to

ANTIBIOTIC TREATMENT:ANTIBIOTIC TREATMENT:

Aqueous penicillin 2million U (IV) + metronidazole 500mg 6hrly

Penicillin V 500mg 4hrly po+ metronidazole 500mg 6hrly orally, Penicillin V 500mg 4hrly po+ metronidazole 500mg 6hrly orally, for additional 4-6 weeksfor additional 4-6 weeks

Ampicillin /sulbactam 1.5-3g I V 6hrlyAmpicillin /sulbactam 1.5-3g I V 6hrly

Amoxacillin/cluvalinic acid (Augmentin) 875/125 mg Amoxacillin/cluvalinic acid (Augmentin) 875/125 mg Orally bid for additional 4-6 weeks Orally bid for additional 4-6 weeks

Clindamycin ,Cefoxitin OR OR

until no symptoms then switch to

Regime 2: For out patient treatment

Clindamycin 600-900mg 6hrly IV ThenClindamycin 600-900mg 6hrly IV ThenClindamycin 300-450mg 6hrly orallyClindamycin 300-450mg 6hrly orally

Cefoxitin(Mefoxin) 1g 8hrly IV Or 2g 4hrly IM Or IVCefoxitin(Mefoxin) 1g 8hrly IV Or 2g 4hrly IM Or IV

Cephalexin (keflex) 500mg 6hrly orally, for 2-4 weeksCephalexin (keflex) 500mg 6hrly orally, for 2-4 weeks

Penicillin V 2g + metronidazole 0.5g 8hrly Penicillin V 2g + metronidazole 0.5g 8hrly orally for 2-4 weeksorally for 2-4 weeks

• Closed wound irrigation-suction: Antibiotic in high concentrations placed in direct

contact with bone manually or implantable pump. Neosporin --- 1% with 0.1% polymyxin B in equal

volume installed on 12 hr cycle.• Antibiotic-impregnated beads: After decortication Tobramycin or Gentamycin

contained in acrylic resin bone cement beads left in place for 10-14 days & then removed

Clindamycin is effective against streptococci & oral anaerobes can also be used with methylmethacrylate.

Local antibiotic therapyLocal antibiotic therapy::

• Intra – arterial antibiotic therapy.

• Local implantation of antibiotic – saturated beads.

• HBO therapy.

1. Incision and drainage:• Incisions made intra orally or extra orally depending

upon location.• In patients with compromised systemic conditions or

toxemia, surgical interference may be post- poned for 2-3 days.

2. Extraction of loose or offending teeth :3. Debridement :

• Following incision and drainage thorough debridement should be done and irrigation with hydrogen peroxide and saline should be done.

4. Decortication : • Obwegesser (1960) advocated this method,

which include removal of chronically infected lateral and inferior cortical plates of bone 1-2 mm beyond the area of involvement, to gain access to Medullary cavity.

5. Sequestrectomy :• Sequestra are usually :

a. Cortical

b. Cancellous

c. Cortico-cancellous

• The Seqeustrum for operative purpose can be classified as :

i. Small and accessible – intra oral approach.

ii. Large and inaccessible – extra oral approach.

6. Saucerization :• Excision of margins of necrotic bone.• Permits visualization and removal of formed and

forming sequestra.• Also smoothen the surface for better soft tissue

adaptation avoiding creation of dead space.

7. Continuous or intermittent indwelling closed catheter irrigation:

• After sequestrectomy or decortication, 2 polyethylene chain tubes, 3-4 mm in diameter and 6-10 inches long are placed through a separate incision.

• One tube is attached to a low pressure suction to allow drainage of pus.

• Another is kept patent to provide irrigation and local antibiotic administration.

• Daily, first saline irrigation followed by antibiotic instillation should be performed until – ve culture are obtained.

8. Trephination or fenestration :• Bony hole or windows are made adjacent to the

infectious process for tissue ammoniation and decompression of the medullary compartment.

9. Resection :• When extensive involvement of bone is seen.

• Can choose various techniques like hemimandibulectomy, segmental resection etc, according to the extent of bone to be removed.

10. Immediate and/or delayed reconstruction:• Is advocated to maintain the continuity of the

fragments.

• To prevent pathological fracture.

• To prevent deformity.

• To provide attachment of soft tissue.

• Short term -100% oxygen inhalation therapy at a pressure greater than that of sea level. The pressure is usually about 2.4 absolute atmospheres or ATA.

• Given as adjuncts for chronic Suppurative and chronic sclerosing osteomyelitis

• 5 days per week 30, 60 or more dive in monophase chamber inhalation of 100% Humidified O2 under pressure at 2.4 ATA for 90mins.

• Each dive is 90 minutes in length

1. Enhancement of lysosomal degradation potential of polymorphoneuclear leucocytes and O2 radicals.

2. Free radicals of O2 radicals are toxic to many pathogenic anaerobes.

3. Many exotoxins liberated by microorganisms are rendered inert by exposure to elevated partial pressure of O2.

4. Tissue hypoxia is intermittently reversed, mimicking tissue level during wound healing.

5. Positive enhancement of neoangiogenesis, in the aerobic portion of proliferative phase of wound healing.

• Decompression sickness

• Elective surgery to prevent clinical radiation necrosis

• Treatment of osteoradionecrosis

• Non healing diabetic ulcers

• Partial reversal of 3-H tissue

• physical mechanism

• dissolution of oxygen into blood

• 80-100 mm Hg range to 1000-1200 mm Hg

• HBO elevates the PAO2

• irrespective of hemoglobin

• O2 gradients -radiated tissue from 50 to 250 mm Hg-macrophage activity

• HBO inhibits inflammation through direct bactericidal effects on anaerobes due to increased production of free radical and toxic products

• HBO enhances phagocytic killing by WBC (Parl 1994)

• Angiogenic and fibroblastic effects- collagen synthesis crucially depends on the availability of molecular O2 that incorporates into a peptide chain to form hydroxyl propyl and hydroxyl lysyl residues.

Protocol of hyperbaric oxygen for elective surgery.

• 20 sessions of hyperbaric oxygen prior to elective surgery, followed by 10 sessions after surgery

• 100% oxygen at 2.4 atmospheric pressure or ATA for 90 treatment minutes

• single person chambers 120 treatment minutes

• The elective surgery protocol is used in all elective surgery in radiated tissue, which may range from tooth extraction, to bone graft reconstruction to vascularized pedicled and free anatomic transfers

• effects of hyperbaric oxygen are permanent,

Contraindications: by HBO committee of the Undersea Medical Society (1988) & Marx (1985)

-Pnemothorax

-Optic neuritis

-Acute viral infections

-Acute Seizures

-Uncontrolled high fever.

-Malignancy.

-H/o Ear or thoracic surgery.

Potential Complications: [Gabb & Robbin 1987]

-Rupture of tympanic membrane.

-O2 Toxicity.

-Eustachian tube dysfunction.

-Pnemothorax.

-Arterial gas embolism.

-Middle ear hemorrhage.

-Deafness.

-Equipment malfunction.

Osteoradionecrosis

• >50Gy radiation kills bone cells

• Nonhealing hypoxic wound

• c/f: trismus fetiod odor, >temp,

• Exposed bone –grey or yellow color

• Fistula

• Pathological #

• Treatment: antibiotics, irrigation, debride

• Most serious complication of radiation therapy.• Probably the first evidence of ORN related to radiotherapy was

reported by Regaud in 1922 • Its pathology was further described by Ewing in 1926, under

the name ‘radiation osteitis’ • Meyer classified ORN as one special type of osteomyelitis. • Titterington also related ORN to osteomyelitis, providing one

of its first definitions, and used the term ‘osteomyelitis of irradiated bone’

• Marx defined it as ‘an area greater than 1 cm of exposed bone in a field of irradiation that had failed to show any evidence of healing for at least 6 months’. He also clarified that in ORN there is no intersticial infection, but only superficial contamination

• An exposure of irradiated bone which fails to heal with out intervention (Marx 1983)

• It is a chronic nonhealing wound caused by hypoxia, hypocellularity, and hypovascularity of irradiated tissue. Marx and Johnson (1987)

• Clinical definition by Van Merkesteyn (1995)

Bone and soft tissue necrosis of 6 months duration excluding radiation induced periodontal breakdown

• Before 1960 orthovoltage -ORN ranging from 17%-37%• megavoltage therapy is bone sparing.• Incidence ranges from upto 10%. When the level of

radiation is less than 60 Gy.• By Reuther et al the incidence was found to be 8.2% in

population of 830 individuals investigated for over a period of 30 years

• Mandible is affected more commonly; because most oral tumors are peri mandibular. More extensive blood supply in maxilla

• Incidence thought to be less after hyperfractionated radiotheryapy at 72-80 Gy or moderately accelerated fractionized radiotherapy of 64-72 Gy.

Radiation beam

Field effect

•greater -central beam

•tapers off -outward

•resemble a target

•center -most affected

•Healing -reduced or absent

1. The affected site should have been previously irradiated;

2. There should be absence of recurrent tumour on the affected site;

3. Mucosal breakdown or failure to heal should occur, resulting in bone exposure (except in cases of bones that lie within thick soft tissue integument’s, such as the pelvis or femur, or rarely in cases of a pathological fracture of the mandible after irradiation);

4. The overlying bone should be ‘dead’, usually due to a hypoxic necrosis;

5. Cellulitis, fistulation, or pathologic fracture need not be present to be considered ORN

• Bone exposure resulting from tumor necrosis where tumor death results in a loss of soft tissue coverage. • bone exposure at the site of tumor during or within

a week of radiotherapy• Bone exposure as a consequence of tumor recurrence.

• In all cases surgical resection was undertaken –tumor recurrence

• Bone exposure resultant from oral surgical or dental interventions. • Extractions sites. Persistent bone necrosis due to denture

irritation • Bone exposure de novo.

• no obvious source of trauma

Int J Oral Maxillofac Surg. 2003 Jun;32(3):289-95

• Osteoradionecrosis of the jaws as a side effect of radiotherapy of head and neck tumor patients--a report of a thirty year retrospective review

• Reuther T, Schuster T, Mende U, Kubler A.

• Retrospective 830 pts

• Incidence 8.2%

• 3 fold higher in Men

• Body of mandible

• Extraction -50%

• Presurgical earlier ORN

• Combined radio and chemo

• Acording to Myers: It is caused due to infection following trauma to jaws after radiation therapy.This hypothesis is no longer accepted.

• According to Marx: It is characterised By 3-H.Radiation

Tissue death due to direct Irreversible cellular Radiation change dysfuntion

HYPOCELLULARITY Damage to bone vascular damage tissue components

Tissue Break down endarteritis and thrombosis

HYPOXIA, HYPOVASCULARITY

Osteoradionecrosis

Loss of reparative function

British Journal of Oral and Maxillofacial Surgery 46 (2008) 653–660

Radiation

generation of ROS

Injured endothelial cells cytokine fibroblasts

Vascular thrombosis atypical myofibroblasts

irreversible DNA Damage

Tissue loss fragile paucicellular cellular fibrosis

replacement

Trauma osteoradionecrosis

• Staging according to MARX:Stage I: Superificial osteoradionecrosis that resolve with irrigation and

HBOStage II: Progressive lesions that Doesn’t heal with Stage I treatmentStage III: Presence of fistulae, pathological fracture or resorptionStage III R: Phase of Early reconstruction after 10 weeks of resection.

• Store and Boysen’s classification of mandibular ORN.Stage Criteria0 Mucosal defects only I Radiological evidence of necrotic bone with intact mucosa II Positive radiographic findings with denuded bone intraorally III Clinically exposed radionecrotic bone, verified by imaging techniques, along with skin fistulas and infection

• HEAD & NECK—DOI 10.1002/hed November 2011

Precipitating factors• Triad

Concept challenged by Gowgiel. Approximately one third of ORN occur spontaneously.

INFECTION

Microbiology

• Cultures streptococci, Candida spp., and gram negative organisms.

• When skin is affected S. aureus and S.epidermidis.

• No organisms are found deep in bone.

• Radiation predisposes to actinomycotic infection; because is favorable environment for microorganism to flourish due to bone tissue alteration

CLINICAL FEATURES

• Within two years

• Asymptomatic dehiscence of mucosa

• Glabrous skin

• As necrosis progresses site more erythematous and severe, deep burning pain

• Evidence of exposed bone

• Tissue surrounding may be ulcerated from infection or recurrent tumor.

• Trismus

• Fetid breath

• Elevated temperature

• Exposed bone with a grey to yellow color

• Intraoral and extra oral fistula

• Pathological fracture

Radiographic changes

• Little-evident

• sequestra or involucra occur late

• radiolucent modeling -nonsclerotic

• Nuclear isotope technetium 99 methylene diphosphonate

• Bony algorithm high resolution CT

Histologically• look like MICROANATOMIC DESERT

• Reduced vascularity, fibrosis

• Diagnosis of osteoradionecrosis should focus primarily on ruling out recurrent or metastatic disease. Therefore is diagnosis of exclusion

Prevention of ORN:

• Through dental Check up

• Through oral prophylaxis

• Extraction of teeth with poor prognosis

• Complete healing of extraction sockets prior to radiation

• Restoration of teeth as required

• Meticulous oral hygiene maintanence

• Correction of any systemic medical disorder

• All invasive and extraction procedures to be avoided for a period of 3 months post radiation therapy

Post irradiation care• Dentures should not be used for one year• Good oral hygiene maintenance • Fluoride therapy • Saliva substitute to prevent dry mouth• Pulpitis- endodontic therapy• Atraumatic extractions –no flap or linear closure• Local anesthetic without adrenaline should be used• Antibiotic should be administered

Management of osteoradionecrosis

• Aim - To control frank infection• Antibiotics • Penicllin plus metronidazole or clindamycin • Supportive therapy with fluids • Pulsating irrigation device can be used. High pressure

should not be used debris might be forced deeply into tissues

• Exposed bone can be mechanically debrided and smoothed with round burs and covered with a pack saturated with zinc peroxide and neomycin

Conservative management of osteoradionecrosis J K Wong, R E Wood, Mc Lean

Triple O 1997; 84:16-21

• local irrigation (saline solution, NaHCO3, or chlorhexidine), systemic antibiotics in acute infectious episodes, avoidance or irritants and oral hygiene instruction.

• Simple management refers to the gentle removal of sequestra in sequestrating lesions

• Had 48% success rates

Treatment of osteonecrotic wounds

• Rule out neoplastic disease • Stabilize the patient medically especially nutritional

status• Preoperative hyperbaric oxygen • Debridement of necrotic mass• Postoperative hyperbaric oxygen • Soft tissue vascular flap support• Bony reconstruction

Ultra sound therapy

• Is non invasive and reportedly promotes neovascularity and neocellularity of ischemic tissues

Major healing of refractory mandible osteoradionecrosis after treatment combining pentoxifylline and tocopherol: a phase II trial.

Head Neck. 2005 Feb;27(2):114-23.Delanian S, Depondt J, Lefaix JL

• Effective in reversing fibronecrotic process

• Eighteen patients

• a daily oral combination of 800 mg of PTX and 1000 IU of vitamin E for 6 to 24 months

• In addition, the last eight patients who were the worst cases were given 1600 mg/day clodronate 5 days

• at 6 months, with 84% healing

• Bedwinek et.al T3 AND T4 lesions - more prone

• higher tissue destruction, larger treatment volume. No necrosis if 50-60Gy used

• Low dosing brachytherapy higher ORN, secondary to decay profile of a combination of mix of alpha, beta and gamma particle spin off.

Stage I 30 x (100% O2 for 90 mins at 2.4 ATA)

Examine exposed bone

No surgery cutaneous fistula No antibiotics

Rinsing only pathologic fracture resorption of Inferior

border of mandible Response

no response10x (100% O2 for 90 mins at 2.4 ATA)Stage I responder

Stage II

Stage III

Stage II

Surgery maintain inferior border

10x (100% O2 for 90 mins at 2.4 ATA)

Response no response

Stage II responder

Healing with out

exposed bone

stage III Excision of nonviable bone Fixation of mandibular segments 10x (100% O2 for 90 mins at 2.4 ATA)

Reconstruction after three months

No HBO Required

REFERENCES

• Oral and Maxillofacial infections – Topazian• Burkets Oral Medicine Diagnosis And Treatment • A text book of Oral Pathology – Shafer• Oral and maxillofacial surgery by Daniel M Laskin.• Oral and maxillofacial Pathology(neville)